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  • 1.
    Abdullahi Mohamed, Mohamed
    Mälardalens högskola, Akademin för hållbar samhälls- och teknikutveckling.
     GLP-1 REGULATES PROLIFERATION OF GLP-1 SECRETING CELLS THROUGH A FEEDBACK MECHANISM2010Independent thesis Advanced level (degree of Master (One Year)), 20 poäng / 30 hpOppgave
    Abstract [en]

    Abstract

    Background and aim:

    Diabetes mellitus (DM) is a chronic and progressive illness that affects all type of populations and ages. According to World health organization (WHO) by 2030 it will be 366 million people effected world wild. Many new drugs are Glucagon-like peptide-1 (GLP-1) based therapy for treatment of type 2diabetes. GLP-1 is released from the intestinal L-cells, and is a potent stimulator of glucose-dependent insulin secretion. The aim of this study was to investigate the effect of GLP-1 and its stable analogs on cell proliferation of GLP-1 secreting GLUTag cells.

    Material and methods:

    GluTag cells were incubated for 48h in DMEM medium containing (0.5% fetal bovine serum and 100 IU/ml penicillin and 100 μg/ml streptomycin and 3mM glucose concentration) in the present or absence of the agents. DNA synthesis was measured using 3H- thymidine incorporation and Ki67 antigen staining. Western blot were performed to investigate the present of GLP-1 receptor in GLUTag cells.

    Results/conclusions:

    These results suggest that GLP-1 regulates proliferation of the GLP-1-secreting cell through a feedback mechanism via its receptor. Since serum GLP-1 levels are decreased in type 2 diabetic patients, the effect of GLP-1 on the GLP-1-secreting cell proliferation suggested here provides a novel beneficial long-term effect of the incretin-based drugs in clinical practice i.e. through increase of the GLP-1-secreting cell mass, augmenting the incretin effect. In addition, the feedback mechanism action of GLP-1 reveals a new insight in regulation manner of the L-cell proliferation.

    GLP-1(7-36) increased cell proliferation in GLUTag cells, an effect which was blocked by the GLP-1 receptor antagonist exendin(9-39). The GLP-1 receptor was expressed in GluTag cells.

    Keywords:

    Incretin hormone, GLP-1, GLP-1 receptor, Exendin-4, Diabetes

    Fulltekst (pdf)
    FULLTEXT01
  • 2.
    Andersson, Per
    et al.
    Mälardalens högskola, Institutionen för vård- och folkhälsovetenskap.
    Sjöberg, RL.
    Uppsala University, Västerås, Sweden .
    Öhrvik, J.
    Uppsala University, Västerås, Sweden .
    Leppert, J.
    Uppsala University, Västerås, Sweden .
    Knowledge about cardiovascular risk factors among obese individuals2006Inngår i: European Journal of Cardiovascular Nursing, ISSN 1474-5151, Vol. 5, nr 4, s. 275-279Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Obesity is an important biological risk factor for cardiovascular disease (CVD). AIMS: The main aim of this study was to answer the question whether obese individuals differ from individuals with normal weight with regard to knowledge about risk factors for CVD. A further aim was to replicate previous findings that obese individuals are at higher risk of developing other biological risk factors for CVD. METHOD: Normal weights, BMI<25 kg/m(2) (n=385), and obese, BMI> or =30 kg/m(2) (n=159), individuals were identified from a screening program conducted among 50-year-old inhabitants of the County of Västmanland, Sweden. Participants answered questions regarding their gender, level of education, and items relating to knowledge about cardiovascular risk factors. Total cholesterol and blood glucose levels, height, weight and blood pressure were measured. RESULTS: Obese individuals did not differ significantly from individuals with a normal weight regarding knowledge of cardiovascular risk factors when education was controlled for. Obesity and low level of education are associated with other risk factors for CVD such as high blood pressure and high serum cholesterol. CONCLUSION: Obese individuals are at an increased risk of developing other risk factors for CVD but are just as knowledgeable about risk factors for CVD as normal weighting individuals.

  • 3.
    Hadrovic, Banina
    Mälardalens högskola, Akademin för hållbar samhälls- och teknikutveckling.
    A study of TRPV1 and TRPV4 ion channels in the beta cells by using fura-2 based microfluorometry.2009Independent thesis Advanced level (degree of Master (Two Years)), 20 poäng / 30 hpOppgave
    Abstract [en]

    The calcium ion (Ca2+) is an important ion that regulates many cellular functions including exocytosis, contraction of muscles, neural functions, fertilization and cell division. In the plasma membrane of cells there are different Ca2+ channels, including the transient receptor potential (TRP) family of cation channels. The TRP channels are activated by physical stimuli like temperature, stretch, osmolality, and also various ligands. These channels are divided into seven subfamilies, namely TRPC, TRPV, TRPM, TRPML, TRPA, TRPP, and TRPN.

     

    TRP channels can regulate the cytoplasmic free Ca2+ concentration ([Ca2+]i)  and are therefore important for research of insulin secretion from beta (β) cells. With TRP research new and more effective treatment methods for people with diabetes can be developed. People with type 2 diabetes have a decreased insulin secretion from beta (β) cells, in response to glucose. Cytoplasmic free Ca2+ concentration ([Ca2+]i)  is important for insulin secretion. It is therefore desirable to find compounds that can increase [Ca2+]i in pancreatic β cells and thereby increase insulin secretion.

     

     

    The aim of this project was to investigate whether pancreatic β cells express TRPV1 and TRPV4 ion channels. If the channels are expressed in β cells the [Ca2+]i can be increased by identifying substances that stimulate TRPV1 and TRPV4 channels. The results can then be used for providing better treatment for patients with diabetes type 2. Insulinoma cells from rat (S5 cells) were used as a model for β cells. [Ca2+]i was measured from single fura-2 loaded S5 cells by ratiometric microfluorometry. To test whether TRPV1 is expressed,

    N-(4-hydroxyphenyl)-Arachidonoylamide (AM404) and [5-hydroxyl-1-(4-hydroxy-3-methoxyphenyl)decan-3-one] ([6]-gingerol) were used. To test whether TRPV4 was expressed, a TRPV4-selective agonist 4alpha-Phorbol 12,13-Didecanoate namely 4α–PDD was used.

     

    The two agonist of TRPV1, AM404 and [6]-gingerol increased [Ca2+]i . Capsaicin a classical activator of TRPV1 used as a control also increased [Ca2+]i . These increases were inhibited by capsazepine, a specific blocker of TRPV1. 4α–PDD, a specific agonist of TRPV4 also increased [Ca2+]i. These results suggest that S5 cells express both TRPV1 and TRPV4 channels and that AM404, [6]-gingerol and 4α–PDD are potential substances for increasing the insulin secretion from β cells.

    Fulltekst (pdf)
    FULLTEXT01
  • 4.
    Rossen, Jenny
    et al.
    Sophiahemmet Högskola.
    Johansson, Unn-Britt
    Sophiahemmet Högskola.
    Lööf, Helena
    Sophiahemmet Högskola.
    Hagströmer, Maria
    Yngve, Agneta
    Exploration of study participants experiences following Sophia Step Study: A two-year physical activity intervention2016Konferansepaper (Annet vitenskapelig)
  • 5.
    Rossen, Jenny
    et al.
    Sophiahemmet Högskola.
    Lööf, Helena
    Sophiahemmet Högskola.
    Yngve, Agneta
    Sophiahemmet Högskola.
    Hagströmer, Maria
    Brismar, Kerstin
    Johansson, Unn-Britt
    Sophiahemmet Högskola.
    Using pedometers for self-management of physical activity: Participants' experiences from Sophia Step Study: A physical activity promotion intervention in pre- and type 2 diabetes2017Konferansepaper (Annet vitenskapelig)
  • 6.
    Tomasic, Nikica
    et al.
    Lund Univ, Dept Clin Sci, Pediat, Klin Gatan 12, S-22184 Lund, Sweden.;Karolinska Univ Hosp, Dept Neonatol, Stockholm, Sweden.;Univ Zagreb, Dept Biol, Fac Sci, Zagreb, Croatia..
    Kotarsky, Heike
    Lund Univ, Dept Pathol, Lund, Region Skane, Sweden..
    Figueiredo, Rejane de Oliveira
    Folkhalsan Res Ctr, Helsinki, Finland..
    Hansson, Eva
    Lund Univ, Dept Clin Sci, Pediat, Klin Gatan 12, S-22184 Lund, Sweden..
    Morgelin, Matthias
    Lund Univ, Dept Clin Sci, Lund, Sweden..
    Tomasic, Ivan
    Mälardalens högskola, Akademin för innovation, design och teknik, Inbyggda system.
    Kallijarvi, Jukka
    Folkhalsan Res Ctr, Helsinki, Finland.;Univ Helsinki, Fac Med, Stem Cells & Metab Res Program, Helsinki, Finland..
    Elmer, Eskil
    Lund Univ, Mitochondrial Med, Dept Clin Sci, Lund, Sweden..
    Jauhiainen, Matti
    Minerva Fdn, Natl Inst Hlth & Welf, Biomedicum 2U, Inst Med Res, Helsinki, Finland..
    Eklund, Erik A.
    Lund Univ, Dept Clin Sci, Pediat, Klin Gatan 12, S-22184 Lund, Sweden..
    Fellman, Vineta
    Lund Univ, Dept Clin Sci, Pediat, Klin Gatan 12, S-22184 Lund, Sweden.;Folkhalsan Res Ctr, Helsinki, Finland.;Univ Helsinki, Childrens Hosp, Helsinki, Finland..
    Fasting reveals largely intact systemic lipid mobilization mechanisms in respiratory chain complex III deficient mice2020Inngår i: Biochimica et Biophysica Acta - Molecular Basis of Disease, ISSN 0925-4439, E-ISSN 1879-260X, Vol. 1866, nr 1, artikkel-id 165573Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Mice homozygous for the human GRACILE syndrome mutation (Bcs1l (c.A232G)) display decreased respiratory chain complex III activity, liver dysfunction, hypoglycemia, rapid loss of white adipose tissue and early death. To assess the underlying mechanism of the lipodystrophy in homozygous mice (Bcs1l(p.S)(78G)), these and wild-type control mice were subjected to a short 4-hour fast. The homozygotes had low baseline blood glucose values, but a similar decrease in response to fasting as in wild-type mice, resulting in hypoglycemia in the majority. Despite the already depleted glycogen and increased triacylglycerol content in the mutant livers, the mice responded to fasting by further depletion and increase, respectively. Increased plasma free fatty acids (FAs) upon fasting suggested normal capacity for mobilization of lipids from white adipose tissue into circulation. Strikingly, however, serum glycerol concentration was not increased concomitantly with free FM, suggesting its rapid uptake into the liver and utilization for fuel or gluconeogenesis in the mutants. The mutant hepatocyte mitochondria were capable of responding to fasting by appropriate morphological changes, as analyzed by electron microscopy, and by increasing respiration. Mutants showed increased hepatic gene expression of major metabolic controllers typically associated with fasting response (Ppargc1a, Fgf21, Cd36) already in the fed state, suggesting a chronic starvation-like metabolic condition. Despite this, the mutant mice responded largely normally to fasting by increasing hepatic respiration and switching to FA utilization, indicating that the mechanisms driving these adaptations are not compromised by the CIII dysfunction. Summary statement: Bcs1l mutant mice with severe CIII deficiency, energy deprivation and post-weaning lipolysis respond to fasting similarly to wild-type mice, suggesting largely normal systemic lipid mobilization and utilization mechanisms.

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